Journal of Ginseng Research最新文献_第2页

Ginsenoside Re mitigates Aβ1-42-induced neurotoxicity by promoting autophagy and suppressing NLRP3 inflammasome 人参皂苷Re通过促进自噬和抑制NLRP3炎性体减轻a β1-42诱导的神经毒性

IF 5.6 2区医学 Q1 CHEMISTRY, MEDICINAL

Journal of Ginseng Research

Pub Date : 2026-01-01 DOI: 10.1016/j.jgr.2025.10.008

Iskander Madhi, Ji-Hee Kim, Hyun Seung Shin, Yun Hee So, Eui-Man Jung, YoungHee Kim

Background

Alzheimer's disease (AD) is a progressive neurodegenerative disorder characterized by β-amyloid (Aβ) accumulation and neuroinflammation. Activation of NOD-like receptor pyrin domain-containing 3 (NLRP3) inflammasome in microglia significantly contributes to AD-associated neuroinflammation and neuronal damage. Ginsenoside Re (G-Re), a major bioactive constituent of Panax ginseng, exhibits anti-inflammatory properties, but its role in modulating inflammasome activation in AD remains unclear.

Methods

This study evaluated the therapeutic potential of G-Re in mice intracerebroventricularly injected with Aβ_1-42 and delineated its molecular mechanisms in complementary cell-based models. We employed behavioral testing, immunohistochemistry, Western blotting, enzyme-linked immunosorbent assays, Annexin V apoptosis assays, and mitochondrial functional assays.

Results

Intraperitoneal administration of G-Re significantly improved cognitive performance, as evidenced by enhanced outcomes in the T-maze and novel object recognition tests. G-Re treatment reduced microglial activation and interleukin-1β (IL-1β) levels in the cortex and hippocampus. In vitro, G-Re protected neurons from conditioned medium derived from Aβ_1-42-stimulated microglia, showing neuroprotection comparable to anti-IL-1β treatment. G-Re also inhibited Aβ_1-42-induced activation of the NLRP3 inflammasome, as indicated by diminished levels of NLRP3, cleaved caspase-1, cleaved gasdermin D (GSDMD), IL-1β, and IL-18 in brain tissues and cultured microglia. Mechanistically, G-Re reduced mitochondrial reactive oxygen species (mtROS), preserved mitochondrial membrane potential, and activated autophagy via SIRT1/AMPK/mTOR signaling, thereby suppressing inflammasome activation.

Conclusion

G-Re ameliorates Aβ_1-42-induced neuroinflammation and cognitive impairment by restoring mitochondrial homeostasis, enhancing autophagy, and suppressing NLRP3 inflammasome activation. These findings suggest G-Re as a potential therapeutic intervention for neurodegenerative disorders including AD.

阿尔茨海默病（AD）是一种以β-淀粉样蛋白（a β）积累和神经炎症为特征的进行性神经退行性疾病。小胶质细胞中nod样受体pyrin结构域3 （NLRP3）炎性小体的激活可显著促进ad相关的神经炎症和神经元损伤。人参皂苷Re （G-Re）是人参的主要生物活性成分，具有抗炎特性，但其在AD中调节炎性体激活的作用尚不清楚。方法本研究评价了Aβ1-42对小鼠脑室注射G-Re的治疗潜力，并在互补细胞模型中描述了其分子机制。我们采用了行为测试、免疫组织化学、免疫印迹、酶联免疫吸附测定、膜联蛋白V凋亡测定和线粒体功能测定。结果经腹腔注射G-Re可显著改善大鼠的认知能力，t迷宫和新物体识别测试的结果均有所提高。G-Re治疗降低了皮质和海马的小胶质细胞活化和白细胞介素-1β (IL-1β)水平。在体外，G-Re保护来自a β1-42刺激的小胶质细胞的条件培养基中的神经元，显示出与抗il -1β治疗相当的神经保护作用。G-Re还抑制了a β1-42诱导的NLRP3炎性体的激活，脑组织和培养的小胶质细胞中NLRP3、cleaved caspase-1、cleaved gasdermin D （GSDMD）、IL-1β和IL-18的水平降低。从机制上说，G-Re减少线粒体活性氧（mtROS），保存线粒体膜电位，并通过SIRT1/AMPK/mTOR信号激活自噬，从而抑制炎症小体的激活。结论- re可通过恢复线粒体稳态、增强自噬、抑制NLRP3炎性体激活等途径改善a β1-42诱导的神经炎症和认知功能障碍。这些发现表明G-Re是包括AD在内的神经退行性疾病的潜在治疗干预手段。

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引用次数: 0

Ginsenoside Rb1 restores dental pulp by promoting odontogenic differentiation of dental pulp stem cells via the TGF-β/Smad signaling pathway 人参皂苷Rb1通过TGF-β/Smad信号通路促进牙髓干细胞成牙分化，从而修复牙髓

IF 5.6 2区医学 Q1 CHEMISTRY, MEDICINAL

Journal of Ginseng Research

Pub Date : 2026-01-01 DOI: 10.1016/j.jgr.2025.11.001

Ok Hyung Nam , Seong Eun Kim , Si Won Kang , Hyekyoung You , Myeong-Kwan Jih , Jaeyoung Ryu , Young Kim

Background

Dental surgery is a common treatment for pulpitis, which can lead to decreased pulp vitality. A novel approach is needed to induce reparative dentin formation without pulp removal. Ginsenoside Rb1 (G-Rb1) is known for its regenerative properties in various diseases. This study aimed to examine the odontogenic differentiation-promoting effects of G-Rb1 in human dental pulp stem cells (hDPSCs) and a rat pulpotomy model, and explore the underlying molecular mechanisms.

Methods

hDPSCs were extracted from supernumerary teeth and cultured with 10 μg/mL G-Rb1. Odontoblastic differentiation was assessed through real-time PCR, western blot, ALP activity, and Alizarin Red S staining. RNA sequencing was performed to confirm the effects of G-Rb1 on odontogenesis of hDPSCs. The effects in the rat pulpotomy model were evaluated by examining reparative dentin formation using von Kossa staining.

Results

G-Rb1 was non-cytotoxic and significantly enhanced hDPSC migration and odontoblastic differentiation in hDPSCs, upregulating the expression of odontogenic markers, DMP1 and DSPP, and increasing mineralized nodule deposition. RNA sequencing identified the TGF-β/Smad pathway as a key mechanism underlying these effects, which was confirmed by evaluating the expression of pathway-related proteins. In vivo analysis demonstrated significantly higher reparative dentin formation in the G-Rb1-treated group compared to the control group.

Conclusion

G-Rb1 promotes odontoblastic differentiation in hDPSCs and enhances reparative dentin formation via the TGF-β/Smad signaling pathway. These findings highlight the potential of G-Rb1 as a therapeutic agent for dental pulp repair and regeneration.

牙髓手术是治疗牙髓炎的常用方法，可导致牙髓活力下降。需要一种新的方法来诱导修复性牙本质的形成而不需要去除牙髓。人参皂苷Rb1 （G-Rb1）因其在多种疾病中的再生特性而闻名。本研究旨在探讨G-Rb1在人牙髓干细胞（hDPSCs）和大鼠断牙模型中促进成牙分化的作用，并探讨其分子机制。方法用10 μg/mL G-Rb1培养多牙dpscs。通过实时荧光定量PCR、western blot、ALP活性和茜素红S染色评估成牙细胞分化。通过RNA测序证实G-Rb1对hdpsc成牙发育的影响。von Kossa染色法观察修复性牙本质形成，评价其对大鼠断髓模型的影响。结果g - rb1无细胞毒性，可显著增强hDPSC在hDPSC中的迁移和成牙细胞分化，上调成牙标志物DMP1和DSPP的表达，增加矿化结节沉积。RNA测序发现TGF-β/Smad通路是这些作用的关键机制，通过评估通路相关蛋白的表达证实了这一点。体内分析表明，与对照组相比，g - rb1处理组的修复性牙本质形成显著增加。结论- rb1通过TGF-β/Smad信号通路促进hDPSCs成牙细胞分化，促进修复性牙本质形成。这些发现突出了G-Rb1作为牙髓修复和再生治疗剂的潜力。

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引用次数: 0

Effects of Korean red ginseng on the HIV-1 env sequence length and CpG dinucleotides 红参对HIV-1 env序列长度和CpG二核苷酸的影响

IF 5.6 2区医学 Q1 CHEMISTRY, MEDICINAL

Journal of Ginseng Research

Pub Date : 2026-01-01 DOI: 10.1016/j.jgr.2025.11.004

Jinny Lee , Seunghee Baek , Young-Keol Cho

Background

Korean Red Ginseng (KRG) and KRG combination therapies have demonstrated long-term benefits in HIV-1-infected patients. This study aimed to assess whether long-term KRG treatment influences sequence length (SL) and CpG700 content in the HIV-1 env gene.

Materials and methods

880 wild-type, full-length env gene sequences were obtained from 482 samples via nested PCR or RT-PCR over a mean duration of 8.0 ± 8.0 years in 200 HIV-1-infected patients. SL and CpG700 content were compared between KRG-naïve (KN, n = 97) and KRG-experienced (KE, n = 103) patients at the time of sequencing, including during the antiretroviral therapy (ART) period. The number of patients with 1, 2, 3 and ≥4 sequenced interval samples was 113, 34, 15, and 38, respectively.

Results

In the whole cohort, the correlation between SL and disease duration (DD) from diagnosis, both before and during ART, was significantly stronger in KE patients than in KN patients (P < 0.01), whereas CpG700 showed no such correlation with DD or KRG. To reduce selection bias, we further analyzed only patients with two or more samples sequenced samples; in this subgroup, both SL and CpG700 demonstrated significant correlations with DD and KRG, with correlation strength increasing as follow-up duration increased. Notably, in the high-intake group receiving prolonged, intensive KRG treatment, CpG700 correlated more strongly with KRG than with DD or SL.

Conclusion

Env SL and CpG700 content are significantly associated with KRG treatment, with the association between KRG and CpG700 becoming more evident over longer follow-up.

韩国红参（KRG）和KRG联合治疗已证明对hiv -1感染患者有长期益处。本研究旨在评估长期KRG治疗是否会影响HIV-1 env基因的序列长度（SL）和CpG700含量。材料与方法从200例hiv -1感染者的482份样本中，通过巢式PCR或RT-PCR获得880个野生型、全长env基因序列，平均持续时间为8.0±8.0年。在测序时比较KRG-naïve （KN, n = 97）和krg经历（KE, n = 103）患者的SL和CpG700含量，包括抗逆转录病毒治疗（ART）期间。有1、2、3和≥4个测序间隔样本的患者分别为113、34、15和38例。结果在整个队列中，KE患者在ART前和ART期间的SL与疾病病程（DD）的相关性显著强于KN患者（P < 0.01），而CpG700与DD或KRG均无相关性。为了减少选择偏差，我们进一步只分析有两个或两个以上样本的患者；在该亚组中，SL和CpG700与DD和KRG均表现出显著的相关性，且随随访时间的增加，相关性增强。值得注意的是，在接受长期强化KRG治疗的高摄入量组中，CpG700与KRG的相关性比与DD或SL的相关性更强。结论env SL和CpG700含量与KRG治疗显著相关，随着随访时间的延长，KRG和CpG700的相关性变得更加明显。

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引用次数: 0

The role of ginseng and ginsenosides in ROS and cardiovascular disease 人参及其皂苷在活性氧和心血管疾病中的作用

IF 5.6 2区医学 Q1 CHEMISTRY, MEDICINAL

Journal of Ginseng Research

Pub Date : 2026-01-01 DOI: 10.1016/j.jgr.2025.08.008

Ajay Vijayakumar, Jun Hong Park, Jong-Hoon Kim

An imbalance in reactive oxygen species (ROS) can lead to severe tissue damage and ultimately result in cell death. While ROS plays a crucial role in cellular signaling, excessive ROS production disrupts intracellular homeostasis, causing oxidative stress, which is a contributing factor to cardiac diseases. Ginseng and its ginsenosides have demonstrated potent antioxidant and cardioprotective properties, and their effectiveness in combating oxidative stress which is closely associated with cardiac health has been thoroughly documented. This review summarizes the cardioprotective roles and molecular mechanisms through which ginseng and its key and rare ginsenosides regulate excess ROS production, restore antioxidant enzyme function, and ameliorate cardiac damage. Key ginsenosides such as Rg1, Rg3, Rb1, and notoginsenoside R1, along with rare forms like Rh1, Rh4, F₂, Mc-1, and TP1 exhibit anti-oxidative property and promote cardiac recovery through both well-established and novel signaling pathways. Recent advances and emerging clinical trial data suggest potential benefits in conditions such as hypertension, ischemia, cardiotoxicity and vascular dysfunction. Collectively, these findings highlight the significance of ginseng and its ginsenoside as valuable adjunct therapy in modern cardiovascular treatment. Further clinical exploration could help translate these preclinical findings into effective cardiac therapies.

活性氧（ROS）失衡可导致严重的组织损伤并最终导致细胞死亡。虽然ROS在细胞信号传导中起着至关重要的作用，但过量的ROS产生会破坏细胞内稳态，引起氧化应激，这是导致心脏病的一个因素。人参及其皂苷已被证明具有有效的抗氧化和保护心脏的特性，它们在对抗与心脏健康密切相关的氧化应激方面的有效性已被充分证明。本文就人参及其关键和稀有人参皂苷调节活性氧过剩、恢复抗氧化酶功能、改善心脏损伤的保护作用及其分子机制进行综述。关键人参皂苷如Rg1、Rg3、Rb1和三七皂苷R1，以及罕见的形式如Rh1、Rh4、F2、Mc-1和TP1表现出抗氧化特性，并通过建立和新的信号通路促进心脏恢复。最近的进展和新出现的临床试验数据表明，它对高血压、缺血、心脏毒性和血管功能障碍等疾病有潜在的益处。总的来说，这些发现突出了人参及其人参皂苷在现代心血管治疗中作为有价值的辅助疗法的意义。进一步的临床探索可能有助于将这些临床前发现转化为有效的心脏治疗方法。

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引用次数: 0

Ginsenoside Rc mitigates hippocampal neuronal damage and cognitive impairment in vascular dementia rats via the pY705-Stat3/Foxo3a and pS727-Stat3/GRIM-19 pathways 人参皂苷Rc通过pY705-Stat3/Foxo3a和pS727-Stat3/GRIM-19通路减轻血管性痴呆大鼠海马神经元损伤和认知功能障碍

IF 5.6 2区医学 Q1 CHEMISTRY, MEDICINAL

Journal of Ginseng Research

Pub Date : 2025-11-01 DOI: 10.1016/j.jgr.2025.07.003

Yuying Wu , Zhizhen Zhang , Xiaoyuan Lian

Background

Vascular dementia (VaD), the second most common cause of dementia, lacks effective treatments. Ginsenoside Rc (GRc) has demonstrated therapeutic potential, but its role in VaD remains unclear. This study investigates the protective effects of GRc in VaD and its underlying mechanisms.

Methods

Cognitive function was assessed using novel object recognition and Morris water maze tests. Neuronal and glial status in the cortex and hippocampus were evaluated by immunohistochemistry, Nissl staining, immunofluorescence, transmission electron microscopy, and Western blotting. Drug target identification was performed through molecular docking, molecular dynamics simulations, and cellular thermal shift assay. Apoptosis markers, along with pY705-Stat3/Foxo3a/Nrf2 and pS727-Stat3/GRIM-19/Sirt1/PGC1α pathway-related factors, were analyzed by cell viability assay, Western blotting, immunoprecipitation, and commercial assay kits.

Results

GRc ameliorated cognitive deficits in VaD rats, attenuating synaptic disruption and neuronal apoptosis in the hippocampal CA1 region. GRc bound to Stat3 and promoted its phosphorylation at Y705 and S727. It further enhanced catalase and SOD activity through pY705-Stat3-mediated Foxo3a activation and upregulated GSR, Gpx4, and GSH via the Nrf2 pathway. Moreover, GRc stabilized the pS727-Stat3/GRIM-19 complex, facilitating mitochondrial translocation of pS727-Stat3, which enhanced mitochondrial Complex I and II activities, increased NAD⁺ levels, and activated the Sirt1/PGC1α pathway, promoting mitochondrial biogenesis and ATP production.

Conclusion

GRc exerted neuroprotective effects in VaD by targeting Stat3 and driving its dual-phosphorylation. Through the pY705-Stat3/Foxo3a and pS727-Stat3/GRIM-19 pathways, GRc alleviated hippocampal neuronal apoptosis and synaptic dysfunction, thereby improving cognitive function in VaD rats.

背景：血管性痴呆（VaD）是痴呆症的第二大常见原因，缺乏有效的治疗方法。人参皂苷Rc （GRc）已显示出治疗潜力，但其在VaD中的作用尚不清楚。本研究探讨GRc对VaD的保护作用及其潜在机制。方法采用新颖的物体识别和Morris水迷宫测试对认知功能进行评估。通过免疫组织化学、尼氏染色、免疫荧光、透射电镜和Western blotting评估皮层和海马的神经元和胶质状态。通过分子对接、分子动力学模拟和细胞热移实验进行药物靶标鉴定。细胞凋亡标志物以及pY705-Stat3/Foxo3a/Nrf2和pS727-Stat3/GRIM-19/Sirt1/PGC1α通路相关因子通过细胞活力测定、Western blotting、免疫沉淀和商用检测试剂盒进行分析。结果grc可改善VaD大鼠的认知缺陷，减轻海马CA1区突触破坏和神经元凋亡。GRc结合Stat3并促进其Y705和S727位点的磷酸化。它通过py705 - stat3介导的Foxo3a激活进一步增强过氧化氢酶和SOD活性，并通过Nrf2途径上调GSR、Gpx4和GSH。此外，GRc稳定了pS727-Stat3/GRIM-19复合体，促进了pS727-Stat3的线粒体易位，从而增强了线粒体复合体I和II的活性，增加了NAD+水平，激活了Sirt1/PGC1α通路，促进了线粒体的生物发生和ATP的产生。结论grc通过靶向Stat3并驱动其双磷酸化发挥VaD的神经保护作用。GRc通过pY705-Stat3/Foxo3a和pS727-Stat3/GRIM-19通路，减轻VaD大鼠海马神经元凋亡和突触功能障碍，从而改善VaD大鼠认知功能。

{"title":"Ginsenoside Rc mitigates hippocampal neuronal damage and cognitive impairment in vascular dementia rats via the pY705-Stat3/Foxo3a and pS727-Stat3/GRIM-19 pathways","authors":"Yuying Wu , Zhizhen Zhang , Xiaoyuan Lian","doi":"10.1016/j.jgr.2025.07.003","DOIUrl":"10.1016/j.jgr.2025.07.003","url":null,"abstract":"<div><h3>Background</h3><div>Vascular dementia (VaD), the second most common cause of dementia, lacks effective treatments. Ginsenoside Rc (GRc) has demonstrated therapeutic potential, but its role in VaD remains unclear. This study investigates the protective effects of GRc in VaD and its underlying mechanisms.</div></div><div><h3>Methods</h3><div>Cognitive function was assessed using novel object recognition and Morris water maze tests. Neuronal and glial status in the cortex and hippocampus were evaluated by immunohistochemistry, Nissl staining, immunofluorescence, transmission electron microscopy, and Western blotting. Drug target identification was performed through molecular docking, molecular dynamics simulations, and cellular thermal shift assay. Apoptosis markers, along with pY705-Stat3/Foxo3a/Nrf2 and pS727-Stat3/GRIM-19/Sirt1/PGC1α pathway-related factors, were analyzed by cell viability assay, Western blotting, immunoprecipitation, and commercial assay kits.</div></div><div><h3>Results</h3><div>GRc ameliorated cognitive deficits in VaD rats, attenuating synaptic disruption and neuronal apoptosis in the hippocampal CA1 region. GRc bound to Stat3 and promoted its phosphorylation at Y705 and S727. It further enhanced catalase and SOD activity through pY705-Stat3-mediated Foxo3a activation and upregulated GSR, Gpx4, and GSH via the Nrf2 pathway. Moreover, GRc stabilized the pS727-Stat3/GRIM-19 complex, facilitating mitochondrial translocation of pS727-Stat3, which enhanced mitochondrial Complex I and II activities, increased NAD<sup>+</sup> levels, and activated the Sirt1/PGC1α pathway, promoting mitochondrial biogenesis and ATP production.</div></div><div><h3>Conclusion</h3><div>GRc exerted neuroprotective effects in VaD by targeting Stat3 and driving its dual-phosphorylation. Through the pY705-Stat3/Foxo3a and pS727-Stat3/GRIM-19 pathways, GRc alleviated hippocampal neuronal apoptosis and synaptic dysfunction, thereby improving cognitive function in VaD rats.</div></div>","PeriodicalId":16035,"journal":{"name":"Journal of Ginseng Research","volume":"49 6","pages":"Pages 702-713"},"PeriodicalIF":5.6,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145435255","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Pharmacokinetics and pharmacological activities of protopanaxatriol 原多巴胺醇的药代动力学及药理活性

IF 5.6 2区医学 Q1 CHEMISTRY, MEDICINAL

Journal of Ginseng Research

Pub Date : 2025-11-01 DOI: 10.1016/j.jgr.2025.07.004

Yeye Hu , Jae Youl Cho , Mi-Yeon Kim

Protopanaxatriol (PPT) is an active metabolite derived from protopanaxatriol-type ginsenosides from Panax ginseng, displaying broad range of pharmacological activities against various diseases with higher efficacy. Since ginsenosides are known to be active components from ginseng, exploring biological activities and functions of the components could be important in terms of understanding ginseng's pharmacological roles. In this review, we aimed to report biological role of PPT by analyzing published literatures and databases. For this purpose, pharmacokinetics and pharmacological activities of PPT, including cardiovascular protection; neuroprotection; skin protection; immunomodulation; and anti-cancer, anti-inflammatory, and anti-diabetes effects were focused. In addition, we also discuss the underlying pharmacological mechanisms of action. This review highlights the importance of PPT for its overall efficacy and aims to inspire further exploration of its diverse potential applications.

原人参醇（PPT）是从人参中提取的一种活性代谢物，对多种疾病具有广泛的药理活性，疗效较高。由于人参皂苷是人参的有效成分，探索人参皂苷的生物活性和功能对了解人参的药理作用具有重要意义。在这篇综述中，我们旨在通过分析已发表的文献和数据库来报道PPT的生物学作用。为此，研究PPT的药代动力学和药理活性，包括心血管保护作用；神经保护;皮肤保护;免疫调节;重点研究了抗癌、抗炎和抗糖尿病的效果。此外，我们还讨论了潜在的药理作用机制。本文综述了PPT在整体疗效方面的重要性，旨在启发进一步探索PPT的多种潜在应用。

引用次数: 0

Protopanaxadiol induces apoptosis through JNK signaling pathway and targeting MLK3 in human melanoma 原甲二醇通过JNK信号通路，靶向MLK3诱导人黑色素瘤细胞凋亡

IF 5.6 2区医学 Q1 CHEMISTRY, MEDICINAL

Journal of Ginseng Research

Pub Date : 2025-11-01 DOI: 10.1016/j.jgr.2025.05.008

Ziliang He , Jae Youl Cho , Daewon Kim

Background

Melanoma is a highly aggressive skin cancer with limited therapeutic options due to drug resistance and recurrence. Protopanaxadiol (PPD), a bioactive metabolite derived from Panax ginseng, has demonstrated promising anticancer properties. However, the effects and underlying mechanisms of PPD on melanoma remain unclear. This study aims to investigate the anticancer effects of PPD on melanoma cells and elucidate its molecular mechanisms.

Methods

To evaluate anti-melanoma activity of PPD and its mechanism MTT and crystal violet staining assays, GO enrichment analysis, KEGG enrichment analysis, flow cytometry, Western blot analysis, and CETSA experiments were carried out.

Results

PPD significantly inhibited the viability of melanoma cells in a dose- and time-dependent manner, inducing morphological changes characteristic of apoptosis. Network pharmacology identified the MAPK signaling pathway as a potential target of PPD, with further confirmation. Inhibition of JNK with SP600125 reversed PPD-induced apoptosis, indicating that JNK signaling plays a critical role. Additionally, PPD specifically activated MLK3, independent of ROS, but not ASK1 or TAK1, which demonstrates that PPD might activate the JNK pathway through targeting and activating MLK3, leading to apoptosis. CETSAs results demonstrated direct binding of PPD to MLK3. Molecular docking and site-directed mutagenesis further indicated the binding site might be LEU248.

Conclusions

Our findings revealed that PPD exerts potent anti-melanoma effects by directly targeting MLK3 and activating the MLK3-JNK signaling pathway, leading to apoptosis. These results provide novel insights into the molecular mechanism of PPD and suggest its potential as a therapeutic agent for melanoma treatment.

黑色素瘤是一种高度侵袭性的皮肤癌，由于耐药和复发，治疗选择有限。原人参二醇（PPD）是一种从人参中提取的生物活性代谢物，具有良好的抗癌作用。然而，PPD对黑色素瘤的作用和潜在机制尚不清楚。本研究旨在探讨PPD对黑色素瘤细胞的抗癌作用，并阐明其分子机制。方法采用MTT、结晶紫染色、GO富集分析、KEGG富集分析、流式细胞术、Western blot分析、CETSA实验等方法评价PPD抗黑色素瘤活性及其机制。结果sppd显著抑制黑色素瘤细胞活力，并呈剂量和时间依赖性，诱导细胞凋亡形态学改变。网络药理学发现MAPK信号通路是PPD的潜在靶点，并进一步证实。SP600125抑制JNK可逆转ppd诱导的细胞凋亡，表明JNK信号在其中起关键作用。此外，PPD特异性激活MLK3，不依赖ROS，但不激活ASK1或TAK1，这表明PPD可能通过靶向和激活MLK3激活JNK通路，导致细胞凋亡。CETSAs结果显示PPD与MLK3直接结合。分子对接和定点突变进一步表明结合位点可能是LEU248。结论PPD通过直接靶向MLK3，激活MLK3- jnk信号通路，导致细胞凋亡，具有较强的抗黑色素瘤作用。这些结果为PPD的分子机制提供了新的见解，并表明其作为黑色素瘤治疗药物的潜力。

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引用次数: 0

Corrigendum to “Saponins from Panax japonicus ameliorate age-related renal fibrosis by inhibition of inflammation mediated by NF-κB and TGF-β1/Smad signaling and suppression of oxidative stress via activation of Nrf2-ARE signaling” [J Ginseng Res, 2021 May;45(3):408–419] “通过抑制NF-κB和TGF-β1/Smad信号介导的炎症和通过激活Nrf2-ARE信号抑制氧化应激，改善年龄相关性肾纤维化”[J] .人参杂志，2021年5月；45 (3): 408 - 419)

IF 5.6 2区医学 Q1 CHEMISTRY, MEDICINAL

Journal of Ginseng Research

Pub Date : 2025-11-01 DOI: 10.1016/j.jgr.2025.08.006

Yan Gao , Ding Yuan , Liyue Gai , Xuelian Wu , Yue Shi , Yumin He , Chaoqi Liu , Changcheng Zhang , Gang Zhou , Chengfu Yuan

引用次数: 0

Pyroptosis: A pharmacological target of ginseng and its phytochemical components for human inflammatory diseases 人参及其植物化学成分对人类炎症性疾病的药理作用靶点

IF 5.6 2区医学 Q1 CHEMISTRY, MEDICINAL

Journal of Ginseng Research

Pub Date : 2025-11-01 DOI: 10.1016/j.jgr.2025.08.001

Young-Su Yi

Pyroptosis is an intensely inflammatory form of lytic programmed cell death, typically triggered by pathogen-associated molecular patterns (PAMPs) and damage-associated molecular patterns (DAMPs) and is likely to form part of the inflammatory responses. It is driven by inflammasome activation during the triggering phase of inflammatory responses rather than the priming phase. Due to its role in inflammation, pyroptosis has been explored as a potential therapeutic target for suppressing inflammatory responses and treating inflammatory diseases. With growing evidence that ginseng and its primary bioactive compounds, ginsenosides, exert anti-inflammatory effects by inhibiting inflammasomes, their potential role in targeting pyroptosis for treating inflammatory diseases is particularly significant. Recent studies have highlighted the inhibitory effects of ginseng and ginsenosides on pyroptosis, along with the underlying mechanisms in inflammatory conditions. This review provides a comprehensive analysis of research investigating the pyroptosis-targeted anti-inflammatory properties of ginseng and ginsenosides, emphasizing their potential as herbal therapeutics for the prevention and treatment of pyroptosis-driven inflammatory diseases.

焦亡是一种强烈炎症形式的溶解性程序性细胞死亡，通常由病原体相关分子模式（PAMPs）和损伤相关分子模式（DAMPs）触发，可能是炎症反应的一部分。它是在炎症反应的触发阶段而不是启动阶段由炎性小体激活驱动的。由于其在炎症中的作用，焦亡已被探索为抑制炎症反应和治疗炎症性疾病的潜在治疗靶点。随着越来越多的证据表明人参及其主要生物活性化合物人参皂苷通过抑制炎症小体发挥抗炎作用，它们在靶向焦亡治疗炎症性疾病中的潜在作用尤为重要。最近的研究强调了人参和人参皂苷对焦亡的抑制作用，以及炎症条件下的潜在机制。本文综述了人参和人参皂苷抗炎特性的研究进展，强调了它们作为预防和治疗由焦热引起的炎症性疾病的草药治疗的潜力。

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引用次数: 0

(20S)-protopanaxatriol attenuates Ang II-induced renal injury via PTPN1-mediated AMPK/mTOR signaling pathway （20S）-protopanaxatriol通过ptpn1介导的AMPK/mTOR信号通路减轻Ang ii诱导的肾损伤

IF 5.6 2区医学 Q1 CHEMISTRY, MEDICINAL

Journal of Ginseng Research

Pub Date : 2025-11-01 DOI: 10.1016/j.jgr.2025.08.009

Risheng Zhao , Zhuoqun Wang , Chang Liu , Linxin Zhang , Min Zhang , Huizhu Du , Gege Yang , Haiming Sun , Wei Liu , Shuang Yan , Mengyang Wang

Background

(20S)-Protopanaxatriol (PPT), a bioactive triterpenoid from Panax ginseng, has been used in Traditional Chinese Medicine (TCM) to tonify kidney yang and regulate blood pressure. The research aimed to elucidate PPT's protective effects against angiotensin II (Ang II)-induced renal injury.

Methods

A C57BL/6 mouse model of kidney injury was established by continuous infusion of Ang II for 4 weeks using an osmotic minipump. Treatment with PPT was initiated two weeks after Ang II infusion and administered daily for 14 days. Molecular docking, drug affinity response target stability (DARTS), and cellular thermal shift assay (CETSA) were employed to identify and validate potential targets of PPT in alleviating Ang II-induced renal injury. Additionally, biochemical assays, histopathological analysis, and Western blotting were performed to assess renal function, tissue damage, and signaling pathway modulation.

Results

Our findings demonstrated that PPT exerted protective effects against Ang II-induced renal dysfunction in mice by significantly attenuating renal fibrosis and inflammation. Mechanistically, PPT targeted PTPN1 and inhibited the AMPK/mTOR signaling pathway, thereby effectively alleviating autophagy dysregulation in both renal tissues of mice and Ang II-stimulated NRK-52E cells in vitro. Molecular docking, DARTS, and CETSA experiments confirmed PTPN1 as a direct target of PPT, providing a molecular basis for its renoprotective effects.

Conclusion

These findings validate ginseng's traditional use in kidney disorders and demonstrate PPT's potential as a therapeutic agent for hypertensive nephropathy by targeting PTPN1/AMPK/mTOR signaling. Further clinical exploration is needed to translate these results into practice.

背景(20S)-原anaxatriol （PPT）是一种从人参中提取的生物活性三萜，在中药中具有补肾阳、调节血压的作用。本研究旨在阐明PPT对血管紧张素II （Ang II）所致肾损伤的保护作用。方法采用渗透小泵连续输注angii，建立C57BL/6大鼠肾损伤模型，持续4周。在Ang II输注后两周开始使用PPT治疗，每天给药，持续14天。采用分子对接、药物亲和反应靶标稳定性（DARTS）和细胞热移测定（CETSA）等方法，鉴定并验证PPT减轻Angⅱ所致肾损伤的潜在靶点。此外，进行生化分析、组织病理学分析和Western blotting来评估肾功能、组织损伤和信号通路调节。结果PPT对angii诱导的小鼠肾功能障碍具有保护作用，可显著减轻肾脏纤维化和炎症。在机制上，PPT靶向PTPN1，抑制AMPK/mTOR信号通路，从而在体外有效缓解小鼠肾组织和angii刺激的NRK-52E细胞的自噬失调。分子对接、dart和CETSA实验证实PTPN1是PPT的直接靶点，为其肝脏保护作用提供了分子基础。结论本研究证实了人参在肾脏疾病中的传统作用，并表明PPT可能通过靶向PTPN1/AMPK/mTOR信号通路作为高血压肾病的治疗药物。将这些结果转化为实践需要进一步的临床探索。

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引用次数: 0